Impaired circadian variations of haemostatic and fibrinolytic parameters in tetraplegia

Iversen, Per Ole; Groot, Patricia D. E.; Hjeltnes, Nils; Andersen, Trine Opstad; Mowinckel, Marie‐Christine; Sandset, Per Morten

doi:10.1046/j.1365-2141.2002.03953.x

Cited by 40 publications

(44 citation statements)

References 24 publications

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“…We observed significant circadian variation in D-dimer and PAI-1, as previously reported [14,15]. After accounting for this variation, an independent effect of DE was not noted at 6 hours after exposure initiation.…”

Section: Discussionsupporting

confidence: 85%

Coagulation markers in healthy human subjects exposed to diesel exhaust

Carlsten

Kaufman

Peretz

et al. 2007

Thrombosis Research

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Background-Ambient particulate matter (PM) is associated with cardiovascular morbidity and mortality. It has been proposed that PM induces a pro-thrombotic process, increasing the risk of cardiovascular events, with some support from epidemiological and laboratory-based models. Diesel exhaust is a major contributor to urban PM, and we conducted a controlled human exposure of diesel exhaust in healthy subjects.

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Section: Discussionsupporting

confidence: 85%

Coagulation markers in healthy human subjects exposed to diesel exhaust

Carlsten

Kaufman

Peretz

et al. 2007

Thrombosis Research

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“…A consistent diurnal variation in FVIII activity has been described. 20 Our values, when corrected for this variation and plotted against %X F8 a still showed a strong linear correlation (R 2 ¼ 0.89, data not shown).…”

Section: Ratiosmentioning

confidence: 88%

“…They are heterozygous for the F8 mutation, and have skewed XCI favouring the activation of the mutant X chromosome (Figure 1). Despite the fact that FVIII activity can be affected by a number of parameters (time of day, 20 age, ABO blood type 22 ) a strong linear correlation was observed in all HA carriers in this family between FVIII activity and the percentage of cells, which have kept the normal X active. These findings demonstrate that HA expression in heterozygous females in this family is due to skewed XCI.…”

Section: Discussionmentioning

confidence: 99%

Heritable skewed X-chromosome inactivation leads to haemophilia A expression in heterozygous females

et al. 2007

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Factor VIII gene, F8, mutations cause haemophilia A (HA), an X-linked recessive disorder. Expression in heterozygous females has been ascribed to skewed X-chromosome inactivation (XCI). To investigate the cause of HA in three heterozygous females within an Atlantic Canadian kindred, the proband (severely affected girl, FVIII activity: 2%) and 17 relatives across three generations were studied. F8 genotype, FVIII activity, XCI ratio (XCIR) (paternal active X: maternal active X), karyotype, submegabase resolution tiling set array competitive genome hybridization (competitive genomic hybridization (SMRT)), and microsatellite analyses were utilized. A positive linear relationship between FVIII activity and percentageactivated normal X-chromosome was found in HA heterozygous females (R 2 ¼ 0.87). All affected, but no unaffected females, had an XCIR skewed toward activation of the mutant X-chromosome (proband 92:8, SD 2). Unexpectedly, high numbers of females have dramatically skewed XCIRs (480:20 or o20:80) (Po0.05). The distribution of XCIR frequencies within this family was significantly different than predicted by normal population data or models of random XCI (Po0.025), with more females having higher degrees of skewing. Known causes of skewing, such as chromosomal abnormalities, selection against deleterious alleles, and X-inactive-specific transcript mutations, are not consistent with our results. This study shows that FVIII activity in HA heterozygous females can be directly related to XCI skewing, and that low FVIII activity in females in this family is due to unfavourable XCI skewing. Further, the findings suggest that these XCI ratios are genetically influenced, consistent with a novel heritable human X controlling element (XCE) functioning similarly to the mouse Xce.

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“…Høyest insidens av dyp venetrombose (38 %) og lungeembolier (5 %) er beskrevet de første tre månede-ne etter skade hos personer med paralytiske tilstander (24). Døgnvariasjonen, som man finner ved plasminogenaktivator-inhibitor 1 (PAI-1), TFPI (tissue factor pathway inhibitor), D-dimer, koagulasjonsfaktorene VII og VIII og protein C og protein S hos funksjonsfriske personer, kan vaere opphevet eller endret hos personer med ryggmargsskade (TFPI, fibrinspaltningsproduktet F 1+2 og Ddimer) (25). Dette kan utgjøre en økt risiko for venøs tromboembolisme hos spinalskadede.…”

Section: Forstyrrelser I Hemostasenunclassified